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  • 1
    ISSN: 1432-0533
    Keywords: Brain ; Incomplete ischemia ; Acidosis ; Light microscopy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Transient severe incomplete ischemia was induced in rats by a combination of bilateral carotid artery clamping and hypovolemic hypotension. Production of lactic acid in the ischemic brain was modified by preischemic administration of glucose or saline. After 30 min of ischemia and 5 or 90 min of recirculation, the animals were fixed by perfusion. High-resolution light microscopy based on whole hemisphere plastic sections revealed that the model produces a highly predictable ischemia in the telencephalon, with a more inconstant injury in the diencephalon, rostral brain stem, and cerebellum. The extent of injury correlates well with studies of local cerebral blood flow in the same model. The present study largely confirmed the opinion, based on the earlier study of the frontoparietal cortex, that the neuronal injury is predominantly of the ‘pale’ type, although fair amounts of ‘dark’ injury also appeared with predilection to the pyriform cortex, hippocampus, and occasionally the cerebellum. Excessive tissue lactic acidosis due to glucose pretreatment aggravated both types of neuronal injury. It was also accompanied by marked astrocytic edema as well as capillary obstruction in the group with long recirculation. A novel type of ischemic tissue change emerged, consisting of osmiophilic granules and whorls probably derived from damaged cell membranes.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 58 (1982), S. 87-94 
    ISSN: 1432-0533
    Keywords: Hypercapnia ; Rat brain ; Ultrastructure ; Cerebral edema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is presently debated how much cellular acidosis contributes to brain cell damage during ischemia and hypoxia. To study the influence of acidosis occurring in the absence of energy failure, extreme hypercapnia was produced in anesthetized, artificially ventilated, and well oxygenated rats by increasing the inspired CO2 concentration until arterialPCO2 reached 150 or 300 mm Hg. At these CO2 tensions intracellular pH falls from a control value of about 7.05 to about 6.85 and 6.65, respectively. After 45 min the brains were fixed in perfusion and processed for light and electron microscopy. AtPaCO2 150 mm Hg no clear neuronal abnormality was detected, but atPaCO2 300 mm Hg some neuronal changes were observed. Notably, the nuclei showed slightly coarser chromatin than normally. In a few nerve cells mild swelling of mitochondria and dispersion of polysomes as well as detachment of ribosomes from the endoplasmic reticulum appeared. In both groups, slight to moderate astrocytic edema developed. Thus, even extreme hypercapnia, with its acompanying marked tissue acidosis, alters ultrastructure in the brain only to such a moderate extent that irreversible cell damage is unlikely. We conclude, therefore, that acidosis occurring during ischemia or hypoxia is detrimental only if pH is further lowered and/or if it occurs in conjunction with cerebral energy failure.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0533
    Keywords: Brain ; Incomplete ischemia ; Acidosis ; Capillaries ; Morphometry
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Excessive tissue lactic acidosis has earlier been shown to aggravate structural damage of both neurons and glial cells in the rat cerebral cortex. To study the reactions of cortical capillaries, light- and electronmicroscopic morphometry was used. Rats were subjected to severe incomplete ischemia (cerebral blood flow below 5% of normal) for 30 min by clamping their carotid arteries and by lowering the blood pressure. Lactate production during ischemia was modified by preischemic administration of either saline (low lactic acidosis group) or glucose (high lactic acidosis group). In the animals with low lactic acidosis, only minimal vascular changes were seen after both 5 min and 90 min recirculation. In the high lactic acidosis group, the endothelial cells were swollen after 5 min of recirculation, and the changes grew markedly worse during 90 min of recirculation. Nuclear chromatin coarsened and mitochondria swelled up. Morphometry showed that the lumen narrowed as a result of endothelial swelling. In spite of variable degree of perivascular astrocytic edema, the outer capillary diameter was little changed in the experimental groups. It seems likely that endothelial swelling hampers postischemic circulation in incomplete ischemia accompanied by high lactic acidosis.
    Type of Medium: Electronic Resource
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